Concurrent upregulation of postsynaptic L-type Ca2+ channel function and protein kinase A signaling is required for the periadolescent facilitation of Ca2+ plateau potentials and dopamine D1 receptor modulation in the prefrontal cortex

Further understanding of how prefrontal cortex (PFC) circuit change during postnatal development is of great interest due to its role in working memory and decision-making, two cognitive abilities that are refined late in adolescence and become altered in schizophrenia. While it is evident that dopamine facilitation of glutamate responses occurs during adolescence in the PFC, little is known about the cellular mechanisms that support these changes. Among them, a developmental facilitation of postsynaptic Ca2+ function is of particular interest given its role in coordinating neuronal ensembles, a process thought to contribute to maturation of PFC function. Here we conducted whole-cell patch clamp recordings of deep-layer pyramidal neurons in PFC brain slices and determined how somatic-evoked Ca2+-mediated plateau depolarizations change throughout postnatal day (PD) 25 (juvenile) to adulthood (PD 80). Postsynaptic Ca2+ potentials in the PFC increase in duration throughout postnatal development. A remarkable shift from short to prolonged depolarizations was observed after PD 40. This change is reflected by an enhancement of L-type Ca2+ channel function and postsynaptic PKA signaling. We speculate that such a protracted developmental facilitation of Ca2+ response in the PFC may contribute to improvement of working memory performance through adolescence.

► Prefrontal L-type Ca2+ plateaus increases throughout postnatal development.
► A significant shift from short to prolonged plateaus was observed after PD 40.
► PKA signaling is required to support this periadolescent facilitation.